AIMS: The hypothesis of this study is that BPD is the result of injury and abnormal repair to an immature lung. We hypothesize that factors involved in the pathogenesis of BPD include abnormalities (congenital or acquired) of the surfactant proteins, oxidative stress, inflammation and cell migration, changes in insulin-like growth factors (IGF's) and elastin components of connective tissue, and pulmonary hypertension with vascular remodeling. AIM 1: To create a Clinical Sample Bank of neonates with lung disease, some of whom will progress to the development of BPD, with a broad clinical database and biostatistical support, to allow basic science investigators in the SCOR project to test hypotheses regarding the pathogenesis of BPD. AIM 2: To determine whether a developmental deficiency of surfactant protein-B (SP-B) contributes to the occurrence of respiratory distress and BPD, and to study metabolic abnormalities associated with inherited deficiency of SP-B. AIM 3: To determine whether plasma nitrotyrosine levels, a marker of peroxynitrite mediated oxidant stress, are elevated in premature infants who develop BPD. AIM 4: To measure the temporal changes in critical components of the inflammatory process (cell composition, inducible nitric oxide synthase (iNOS), hyaluronan (HA), and Receptor for HA-mediated mobility (RHAMM), and selected cytokines) in bronchoalveolar lavage (BAL), blood, and urine samples obtained from intubated infants with lung disease, and to correlate these changes with their clinical course. AIM 5: To examine changes in the IGF axis that occurs in lungs of infants with RDS and BPD. AIM 6: To determine whether there is a relationship between degradation of elastin, as determined by assay of elastin-derived peptides in BAL samples, and the clinical course of BPD. AIM 7: To determine whether the normal fall in plasma endothelin-1 concentrations after birth are delayed in infants with RDS and BPD.